The purpose of this proposal is to study the regulation of renal acid excretion. Emphasis is placed on a new theory which views the renal response to chronic acid-base disorders to be governed by "non-pH-homeostatic" factors. Specific questions include: 1. Interplay of volume regulation and acid excretion in chronic acid-base disorders. a. Does volume contraction impede acid excretion during prolonged HCl feeding? b. Does vena cava constriction influence the response to chronic HCl loads? c. Does reduced proximal Na reabsorption alter the renal response to HCl loading? d. Does proximal Na reabsorption influence the response to changes in PaCO2? 2. Role of mineralocorticoid-induced changes in Na avidity in the increased H ion secretion elicited by acid feeding and by chronic hypercapnia. a. Does prolonged H2SO4 or HNO3 feeding cause aldosterone levels to rise? b. Does aldosterone play a role in the renal response H2SO4 or HNO3 feeding? c. Does DOCA without dietary Na facilitate the response to acid feeding? d. Does aldosterone play a role in the renal response to chronic hypercapnia? 3. Role of renal ammoniogenesis as an obstacle to accelerating acid excretion. a. Is there a delay in the renal response to the H ion load of monobasic phosphate? b. Does prior sodium depletion alter the renal response to sulfuric acid loading? c. Is the response to H ion loads altered by repeated intervals of H2SO4 feeding? d. Does prior augmentation of NH4 ion excretion alter the renal response to H2SO4? 4. Influence of the dietary anion mixture on steady-state acid-base equilibrium in normals, acid-fed animals and animals with chronic renal insufficiency. a. What is the relationship of steady-state (HCO3) and NaCl intake during H2SO4 feeding? b. Do dietary anions influence normal acid-base balance? c. Do dietary anions influence acid-base balance in chronic renal failure?